There is now considerable evidence that even ambient oxygen may impose a stress on the organism under certain circumstances. Oxygen centered radicals have been implicated in a wide variety of pathologies. For instance, the chain reaction chemistry initiated by free radicals has recently been suggested as the initiating mechanism which results in tissue damage during the reoxidation phase subject to ischemica. On the one hand increased oxygen extraction is recognized as a potent stress while on the other, endurance exercise is often advocated as a means of improving the oxygen consumption of a sedentary population. At present, it is not at all clear how the organism tolerates the increased oxygen centered radicals which are known to be generated during exercise. Since exercise and other stressors, such as cold, stimulate increased oxygen flow through the tissue or produce intermittent hypoxia and normoxia they should provide a potent model for studying the organism's mechanisms of defense against active oxygen. This proposal outlines research designed to determine: (1) whether a similar mechanism operates to reduce lipid peroxidation in animals exposed to exercise or cold (2) whether tissue consumption of lipid peroxides is an important mechanism of adaptation to increased oxygen consumption, (3) whether beta-blockers function in vivo to reduce lipid peroxidation. This research differs from previous studies related to whole organism oxygen consumption and lipid peroxidation in that it will: (1) avoid the inherrent problems of using malonaldehyde as the sole criterion for tissue lipid peroxidation, (2) study lipid peroxide metabolism which has largely been ignored and (3) include functional measurements of the whole organism's behavior.